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REVIEW ARTICLE

Do glial cells play an anti-oxidative role in Huntington's disease?

, , , , , , & show all
Pages 1135-1144 | Received 13 May 2014, Accepted 16 Jun 2014, Published online: 14 Aug 2014
 

Abstract

Oxidative stress is a condition of imbalance between reactive oxygen species (ROS) formation and antioxidant capacity as a result of dysfunction of the antioxidant system. ROS can be served as a second messenger at low or moderate concentration, while excessive amount of ROS under oxidative stress condition would destroy macromolecules like proteins, DNA, and lipids, finally leading to cell apoptosis or necrosis. Changes in these macromolecules are involved in various pathological changes and progression of diseases, especially neurodegenerative diseases. Neurodegenerative diseases are morphologically featured by progressive neuronal cell loss, accompanied with inclusions formed by protein aggregates in neurons or glial cells. Neurons have always received much more attention than glial cells in neurodegenerative diseases. Actually, glial cells might play a key role in the functioning of neurons and cellular survival through an antioxidant way. Additionally, neurons can modulate the activities of glia either. Herein, the main purposes of this review are to mention the connection between Huntington's disease (HD) and oxidative stress, to summarize the characteristics and functions of glial cells in HD, to state the cross talk between neurons and glial cells, and to emphasize the conclusive role of activation of Keap1-Nrf2-ARE pathway in glial cells against oxidative stress in HD.

Acknowledgements

This work was supported by the National Natural Science Foundation of China (Nos. 81274122, 81102831, 81173578, 81202507, 81273629, 81373510), the National Key Sci-Tech Major Special Item (No. 2012ZX09301002-004, No. 2012ZX09103101-006), the National High-Tech R&D Programme (863 Program) (No. 2012AA020303), the Program for Changjiang Scholars and Innovative Research Team in University (PCSIRT) (No. IRT1007), the Specialized Research Fund for the Doctoral Program of Higher Education of China (No. 20121106130001), Beijing Natural Science Foundation (Nos. 7131013, 7142115), Beijing Key Laboratory of New Drug Mechanisms and Pharmacological Evaluation Study (No. BZ0150), PUMC Youth Fund, Fundamental scientific research funds for central public institute (No. 2014RC03).

Declaration of interest

The authors report no declarations of interest. The authors alone are responsible for the content and writing of the paper.

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